Sunday, August 28, 2011

A Note On Mode of action of fluoride and the caries process

The use of fluorides date back to as early as 1874 when the German Erharde suggested the use of potassium fluoride tablets for expectant mothers and children in order to strengthen teeth. This recommendation was without any scientific evidence. What we now know to be dental fluorosis (mottling) was noted by dentists long ago who reported on 'Colorado Stain' without the aetiology of the tooth defect being established.

Mode of action of fluoride and the caries process

The mineral of tooth tissues exists as a carbonated apatite, which contains calcium, phosphate, and hydroxyl ions, making it a hydroxyapatite [Ca10.(PO4)6.(OH)2]. Carbonated portions weaken the structure and render the tissue susceptible to attack. Food remnants and debris mix with saliva and adhere to tooth surfaces as a slimy film known as dental plaque. Oral bacteria, and most importantly certain types of cariogenic bacteria (e.g. Mutans streptococci and Lactobacilli species), metabolize dental plaque and produce acid which lowers the pH of the oral environment. When the pH is below the critical pH for hydroxyapatite (
5.5), demineralization occurs with a net outward flow of calcium and phosphorous ions from the enamel surface into plaque and saliva. 

When the pH returns to 7.0, remineralization occurs with a net inward flow of ions into the enamel surface. If fluoride is present during remineralization, it is incorporated to form fluorapatite [Ca10.(PO4)6.F2], which is more stable and resistant to further acid attacks. The process of demineralization and remineralization is an ongoing one and frequently referred to as 'the ionic see-saw' or 'tug-of-war'. This is now widely believed to be the most important preventive action of fluoride, and a constant post-eruptive supply of ionic fluoride is thought to be most effective.

A number of mechanisms have been proposed to explain the action of fluoride.

The first is that fluoride has an effect during tooth formation by substitution of hydroxyl ions for fluoride ions, thereby reducing the solubility of the tooth tissues.

Second, fluoride can inhibit plaque bacterial growth and glycolysis. At pH 7.0, fluoride ions are precluded from entering bacteria. However, at pH 5.0, fluoride exists as hydrofluoric acid, which crosses the bacterial cell membrane to interfere with its metabolism, by specifically inhibiting the enzyme enolase in the glycolytic pathway. 

Third fluoride inhibits the demineralization of tooth mineral when present in solution at the tooth surface. 

Fourth, fluoride enhances remineralization by combining with calcium and phosphate to form fluorapatite. Fluoride enhances crystal growth, stabilizes and makes the tissue resistant to further acid attack.

Enamel apatite demineralizes when the pH drops to pH 5.5. However, when fluorapatite is formed during remineralization, it is even more resistant to demineralization as the critical pH for fluorapatite is pH 3.5. Therefore, it is most important to have an intraoral source of fluoride when remineralization is taking place. Lastly, fluoride affects the morphology of the crown of the tooth, making the coronal pits and fissures shallower. Such shallower pits and fissures will be less likely to collect food debris, allow stagnation and become decayed. The most important of these mechanisms is that when fluoride is present in the oral environment at the time of the acid attack it inhibits demineralization and promotes remineralization.

As early as 1890, Miller drew attention to the dissolutive process of dental caries and directed efforts to inhibit dissolution. The clinical findings of the anti-caries activity of drinking water with fluoride caused researchers to seek reasons for this. The finding that fluoride-treated enamel had a lower solubility led many to consider this as a cause and effect relationship. The anti-caries action of fluoride was thought to be one of preventing dissolution of enamel, and efforts were made to incorporate more and more amounts of fluoride into surface enamel. 

The first topical agent used, after water fluoridation, was a 2% sodium fluoride solution and there was a greater uptake of fluoride into enamel from acidified solutions. Numerous fluoride preparations with varying concentrations of fluoride were employed for topical application and used as anti-caries agents. It was noted that there was not much difference in the caries reductions reported from the topical fluoride studies despite great variations in the fluoride concentrations used. In addition, the difference in the levels of fluoride in surface enamel of residents of fluoridated and non-fluoridated areas was limited. Therefore, it is difficult to explain the 50% reduction of caries observed, on the basis of the fluoride level in the surface enamel. Furthermore, there has been no study to show any clear-cut inverse relationship between fluoride content of surface enamel and dental caries.

All the available evidence is that caries results from the presence of an acidogenic plaque on elements of the tooth mineral. The diffusion of acidic components into the tooth mineral is accompanied by the reverse diffusion of components of the mineral. During the carious process there is a preferential loss of calcium, accompanied by dissolution of magnesium and carbonate. The first clinical sign of enamel caries is the so-called 'white spot' lesion, where an apparently sound surface overlies an area of decalcification. The remineralization effect of fluoride has since come into favour. It has been reported that attacked enamel could re-harden on exposure to saliva and that softened enamel could be re-hardened by solutions of calcium phosphates in vitro. However, it is now known that it is the presence of fluoride in the oral cavity, and in particular, its presence in the liquid phase at the enamel-plaque interface, that is of most importance.

In the past it was thought that the systemic action of fluoride was important for caries prevention. This view has completely changed and it is now known that it is the topical action of fluoride that is essential for caries prevention. It is the presence of fluoride in the liquid phase at the plaque-enamel interface that is of most importance. Studies have shown that even low levels of fluoride (0.10 ppm) were effective in preventing the dissolution of enamel. It has been stated that the activity of the fluoride ion in the oral fluid that is important in reducing the solubility of the enamel rather than a high content of fluoride in the enamel. Saliva, the fluid that bathes the teeth has been extensively studied. The level of fluoride in saliva is thought to be important for caries prevention and it has been shown that caries susceptible subjects had salivary fluoride levels of <
0.02 ppm, whereas caries resistant subjects had levels of >0.04 ppm.

Key Points
· It is the activity of the fluoride ion in the oral fluid that is of most importance in reducing enamel solubility rather than having a high content of fluoride in surface enamel.
· A constant supply of low levels of intraoral fluoride, particularly at the saliva/ plaque/enamel interface, is of most benefit in preventing dental caries.

There are a vast number of fluoride products that are available for systemic and topical use. They can be applied professionally by the dental team or by the patient at home.


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